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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-8-18
pubmed:abstractText
We demonstrate here that the CD44 molecule, which mediates lymphocyte adhesion to high endothelial venules (HEV), is also involved in the delivery of an activation signal to the T cell. We have produced a CD44 mAb (H90) which is able to block the binding of lymphocytes to high endothelial venules. H90 had no effect on [3H]TdR incorporation of whole PBL stimulated by lectins, allogeneic cells, or CD3 mAb in the soluble phase; in contrast, it strongly increased [3H]TdR incorporation of PBL stimulated by CD2 pairs of mAb or by CD3 mAb linked to the plastic culture plates, when purified T cells were used, H90 mAb could efficiently induce them to proliferate after a primary signal of activation delivered via cross-linked CD3 or via CD2, an effect mediated by Il-2 synthesis and Il-2R expression. Thus, the effect of H90 mAb resembles the mitogenic effect of CD28 "9.3" mAb. However, several results show that CD28 and CD44 mediate different signals to the T cells: i) in contrast to CD28 mAb, CD44 mAb cannot complement the signal delivered by a soluble CD3 mAb, lectins, or PMA; ii) CD44 mAb, at the difference of CD28 mAb, cannot induce CD3+ thymocytes to proliferate in conjunction with a first signal provided via cross-linked CD3 or via CD2; iii) F(ab) fragments of H90 were efficient, whereas divalent fragments of CD29 9.3 mAb are required to produce activation signals; and iv) CD44 and CD28 mAb produce a very strong synergistic effect on T cell proliferation. These results fit with previous ones showing that endothelial cells can play the role of accessory cell in T cell activation and that a hierarchy of signaling can be delivered to T cells via CD3 and CD2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD2, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD27, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation..., http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface, http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lymphocyte Homing
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
143
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
798-801
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:2568380-Adjuvants, Immunologic, pubmed-meshheading:2568380-Animals, pubmed-meshheading:2568380-Antibodies, Monoclonal, pubmed-meshheading:2568380-Antigens, CD2, pubmed-meshheading:2568380-Antigens, CD27, pubmed-meshheading:2568380-Antigens, CD3, pubmed-meshheading:2568380-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:2568380-Antigens, Surface, pubmed-meshheading:2568380-Binding, Competitive, pubmed-meshheading:2568380-Binding Sites, Antibody, pubmed-meshheading:2568380-Cell Adhesion Molecules, pubmed-meshheading:2568380-Endothelium, Lymphatic, pubmed-meshheading:2568380-Humans, pubmed-meshheading:2568380-Lymphocyte Activation, pubmed-meshheading:2568380-Mice, pubmed-meshheading:2568380-Molecular Weight, pubmed-meshheading:2568380-Receptors, Antigen, T-Cell, pubmed-meshheading:2568380-Receptors, Immunologic, pubmed-meshheading:2568380-Receptors, Lymphocyte Homing, pubmed-meshheading:2568380-T-Lymphocytes
pubmed:year
1989
pubmed:articleTitle
CD44 contributes to T cell activation.
pubmed:affiliation
Laboratoire d'Immunologie des Tumeurs de l'Enfant, Institut Gustave-Roussy, Villejuif, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't